CRMP4a suppresses cell motility by sequestering RhoA activity in prostate cancer cells

Li, Changlin; Xu, Haixia; Xiao, Lin; Zhu, Haizhou; Zhang, Guoan; Wei, Wei; Li, Kaizhi; Cao, Xiande; Shen, Daqing; Holzbeierlein, Jeffrey M.; Li, Benyi

doi:10.1080/15384047.2018.1491507

Cited by 6 publications

(4 citation statements)

References 29 publications

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“…Rhosin (30 μM [Li et al, 2018; Privat et al, 2020; Yao et al, 2017], HY‐12646A, MedChemExpress, Newark, NJ) is a potent and specific RhoA subfamily Rho GTPase inhibitor that specifically binds to RhoA and was dissolved in dimethyl sulfoxide (DMSO). Rhosin was added to the medium during OGD/R treatment.…”

Section: Methodsmentioning

confidence: 99%

EphA4 regulates white matter remyelination after ischemic stroke through Ephexin‐1/RhoA/ROCK signaling pathway

Liu

Han

Zheng

et al. 2022

Glia

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Ischemic stroke, which accounts for nearly 80% of all strokes, leads to white matter injury and neurobehavioral dysfunction, but relevant therapies to inhibit demyelination or promote remyelination after white matter injury are still unavailable. In this study, the middle cerebral artery occlusion/reperfusion (MCAO/R) in vivo and oxygen–glucose deprivation/reoxygenation (OGD/R) in vitro were used to establish the ischemic models. We found that Eph receptor A4 (EphA4) had no effect on the apoptosis of oligodendrocytes using TUNEL staining. In contrast, EphA4 promoted proliferation of oligodendrocyte precursor cells (OPCs), but reduced the numbers of mature oligodendrocytes and the levels of myelin‐associated proteins (MAG, MOG, and MBP) in the process of remyelination in ischemic models in vivo and in vitro as determined using PDGFRα‐EphA4‐shRNA and LV‐EphA4 treatments. Notably, conditional knockout of EphA4 in OPCs (EphA4fl/fl + AAV‐PDGFRα‐Cre) improved the levels of myelin‐associated proteins and functional recovery following ischemic stroke. In addition, regulation of remyelination by EphA4 was mediated by the Ephexin‐1/RhoA/ROCK signaling pathway. Therefore, EphA4 did not affect oligodendrocyte (OL) apoptosis but regulated white matter remyelination after ischemic stroke through the Ephexin‐1/RhoA/ROCK signaling pathway. EphA4 may provide a novel and effective therapeutic target in clinical practice of ischemic stroke.

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Section: Methodsmentioning

confidence: 99%

EphA4 regulates white matter remyelination after ischemic stroke through Ephexin‐1/RhoA/ROCK signaling pathway

Liu

Han

Zheng

et al. 2022

Glia

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“…Real-time PCR was performed as in our previous studies. 29 Briefly, total RNA was extracted from cells using the Trizol reagent (Invitrogen) following the manufacturer's instructions. 1 µg RNA was subjected to reverse transcription (RT) using a 5× All-In-One RT MasterMix reverse Transcription Kit (ABM Company, Canada).…”

Section: Real Time Pcrmentioning

confidence: 99%

“…Lentivirus were packaged as described before. 29 Briefly, psPAX2/pMD2.G (Addgene, catalog # 12259, 12260) and pLVX-puro-cOVA vector were co-transfected into 293 T cells. These RM-1 cells were subjected to infection with supernatants containing the lentivirus and were then selected using puromycin (Gibco, catalog #A1113802, 1 μg/ml).…”

Section: Rm-1-oval (Chicken Ovalbumin) Cells Constructsmentioning

confidence: 99%

Alternol triggers immunogenic cell death via reactive oxygen species generation

Zhang

Yan

et al. 2021

OncoImmunology

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Alternol is a naturally occurring compound that exerts antitumor activity in several cancers. However, whether Alternol induces antitumor immune response remains unknown. In this study, we investigated whether Alternol induced immunogenic cell death (ICD) in prostate cancer cells. Alternol triggered ICD in prostate cancer cells, as evidenced by the release of damage-associated molecular patterns (DAMPs) (i.e., calreticulin, CALR; high mobility group protein B1, HMGB1; and adenosine triphosphate, ATP) and proinflammatory cytokine (i.e., interleukin [IL]-1α, IL-1β, IL-6, and IL-8) expression. Alternol facilitated tumorassociated antigen uptake and cross-presentation, CD8 + T-cell priming, and T-cell infiltration in tumordraining lymph nodes (LNs) and tumors. The presence of Alternol fostered antitumor immune response in vivo, resulting in delayed tumor growth and prolonged survival. Moreover, inhibition of reactive oxygen species (ROS) generation blocked Alternol-induced upregulation of pre-inflammation cytokines, endoplasmic reticulum (ER) stress, and consequent antitumor immune response. Overall, our data indicate that Alternol triggers ICD in prostate cancer cells, which is mediated by ROS generation.

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“…Single guide RNA (sgRNA) anti-XPA was cloned into lentiCRISPR V2 (Addgene plasmid #52961) using Bsm BI restriction enzyme sites [ 60 ]. Small hairpin interfering RNAs (shRNA) against XPA were cloned into PLKO.1-puro vector (Addgene Plasmid #8453) using AgeI/EcoRI restriction enzyme sites [ 61 ]. PAX2, pMD2.G (Addgene plasmid #12259-12260), and lenti-CRISPR V2 expressing sgRNA were co-transferred into 293 T cells.…”

Section: Methodsmentioning

confidence: 99%

Idarubicin combats abiraterone and enzalutamide resistance in prostate cells via targeting XPA protein

Zhang

Wei

et al. 2022

Cell Death Dis

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Although second-generation therapies like abiraterone (ABI) and enzalutamide (ENZ) benefit patients with castration-resistant prostate cancer (CRPC), drug resistance frequently occurs, eventually resulting in therapy failure. In this study, we used two libraries, FDA-approved drug library and CRISP/Cas9 knockout (GeCKO) library to screen for drugs that overcome treatment resistance and to identify the potential drug-resistant genes involved in treatment resistance. Our screening results showed that the DNA-damaging agent idarubicin (IDA) overcame abiraterone and enzalutamide resistance in prostate cancer cells. IDA treatment inhibited the DNA repair protein XPA expression in a transcription-independent manner. Consistently, XPA knockout sensitized prostate cancer cells to abiraterone and enzalutamide treatment. In conclusion, IDA combats abiraterone and enzalutamide resistance by reducing XPA protein level in prostate cancer.

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CRMP4a suppresses cell motility by sequestering RhoA activity in prostate cancer cells

Abstract: Our data demonstrated that CRMP4a interacts with RhoA and sequesters its activity, resulting in suppression of cytoskeletal organization, cell migration and spreading.

Cited by 6 publications

References 29 publications

EphA4 regulates white matter remyelination after ischemic stroke through Ephexin‐1/RhoA/ROCK signaling pathway

EphA4 regulates white matter remyelination after ischemic stroke through Ephexin‐1/RhoA/ROCK signaling pathway

Alternol triggers immunogenic cell death via reactive oxygen species generation

Idarubicin combats abiraterone and enzalutamide resistance in prostate cells via targeting XPA protein

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